Changes in the urinary excretion of beta2-microglobulin (beta 2MG) and N-acetyl-beta-D-glucosaminidase (NAG) during treatment for lupus nephritis.
Division of Nephrology, Department of Internal Medicine, Jichi Medical University, Shimotsuke, Japan.Internal Medicine (Impact Factor: 0.9). 02/2008; 47(4):287-90.
Tubulointerstitial involvement in the kidneys is frequently found but it is a less emphasized feature of lupus nephritis (LN). Recent studies have shown increases in the urinary excretion of beta2-microglobulin (beta 2MG) and N-acetyl-beta-D-glucosaminidase (NAG), which are considered to indicate the presence of tubulointerstitial damage, particularly in cases of LN. However, the changes in these urinary parameters during the clinical course of LN have not yet been fully clarified. In this report, we describe the changes in the urinary excretion of beta 2MG and NAG during immunosuppressive treatment combined with double filtration plasmapheresis in a case of LN.
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ABSTRACT: Evaluation of specific urinary markers with respect to urine creatinine (uCreat) is common. However, as uCreat is a function of both glomerular filtration and tubular secretion, using uCreat for specific tubular markers, suggests that glomerular function is normal, and there is no tubular secretion. Thus, adjusting values of any tubular marker to uCreat, especially in patients with acute or even moderate chronic renal failure, can be misleading. Using urine cystatin-C (uCST3) as a model tubular marker for following 120 kidney graft recipients daily, we evaluated the utility of either uCST3 alone or the uCST3/uCreat ratio to detect tubular damage. All positive kidney biopsies were always associated with a uCST3>0.18 mg/L. Using the uCST3/uCreat ratio, discrepancies regarding biopsy status were observed in nine patients (4 false positive, 5 false negative results). In two patients, variability of uCreat appeared to be the most important factor causing inconsistent uCST3/uCreat ratios. With a negative predictive value (NPV) of 85.7%, uCST3/uCreat can lead to errors in clinical interpretation. These errors can be avoided when estimates of tubular damage are based on uCST3 concentrations alone (NPV=100%). We recommend using the uCST3 value to evaluate the extent of renal tubular damage. Indeed, our conflicting results on uCST3/uCreat can be extended to every marker of tubular function. Evaluating a urine marker specific for renal tubular damage to a second urine marker that is itself strongly dependent upon glomerular or other renal or non-renal conditions, impairs its clinical relevance and may lead to incorrect interpretations. Correction with uCreat can be performed only in pure glomerulopathy, when specific markers of glomerular function are measured (i.e., urinary albumin). In all other cases of renal diseases, such correction is inappropriate and should be avoided. Clin Chem Lab Med 2009;47:1553-6.Clinical Chemistry and Laboratory Medicine 10/2009; 47(12):1553-6. DOI:10.1515/CCLM.2009.341 · 2.71 Impact Factor
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ABSTRACT: Although the clinical benefits of antiviral treatment in the management of membranous nephropathy (MN) in patients with chronic hepatitis B virus (HBV) infection have been suggested, it should be evaluated more carefully. In this report, we present two cases with quiescent HBV who were administered lamivudine for either the initial treatment of MN or to control the reactivation of HBV during treatment with corticosteroids. No clinical benefit of lamivudine as an initial treatment was observed in one patient, which obliged us to commence administration of prednisolone (PSL). On the other hand, lamivudine seemed to play a pivotal role in the remission of an acute exacerbation of hepatitis B during treatment with PSL and mizoribine in the other patient. These two patients seemed to tolerate administration of PSL with or without an immunosuppressive agent well, since gradual and prompt improvements of nephrotic status were confirmed within a few months, thus suggesting the potential benefit of steroid treatment. There is little consensus regarding the optimal choice of steroids and immunosuppressants for the treatment of MN with chronic HBV infection, due to the potential for stimulation of viral replication and precipitation of hepatic flares. Our observations, however, suggest that treatment with PSL still should be reserved for quiescent HBV carriers with MN. Further studies will be required to determine the optimal timing and appropriate duration of antiviral treatment in such patients requiring long-term immunosuppression.Clinical and Experimental Nephrology 04/2011; 15(2):289-93. DOI:10.1007/s10157-010-0391-z · 2.02 Impact Factor
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ABSTRACT: In ordinary settings, human immunodeficiency virus (HIV)-associated nephropathy should be considered when HIV infection is associated with heavy proteinuria. On the other hand, hepatitis B virus (HBV) may also play a role in the development of glomerular injury among patients with HIV infection, since HIV and HBV infections commonly occur together due to shared modes of transmission. We present here a case of nephrotic syndrome in an HIV-positive patient complicated with HBV infection. A renal biopsy revealed sparse granular deposits of immunoglobulin G in the subepithelial region, consistent with membranous nephropathy (MN) stage I. Moreover, immunostaining exhibited weak anti-hepatitis B core activity within glomeruli. These results led us to consider that HBV-associated MN might play a role in the development of nephrotic syndrome. Although anti-viral treatment for patients with HBV-associated MN has been suggested to be clinically effective, the use of two anti-HIV agents (tenofovir and emtricitabine), both of which have anti-HBV activities, was not effective for the patient's nephrotic syndrome, despite obtaining a decrease in the serum HBV-DNA levels. A lack of prospective data suggests that many decisions on the treatment of glomerulopathies with HIV infections are potentially empirical. Obviously, further studies and accumulated clinical experience are required to better determine the pathogenesis and management of HBV-associated MN among patients with HIV infections.Clinical and Experimental Nephrology 06/2011; 15(5):769-73. DOI:10.1007/s10157-011-0477-2 · 2.02 Impact Factor
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